Zhu, Y., Wang, D., Wang, F., Li, T., Dong, L., Liu, H., Ma, Y., Jiang, F., Yin, H., Yan, W., Luo, M., Tang, Z., Zhang, G., Wang, Q., Zhang, J., Zhou, J., and Yu, J. (2013) A comprehensive analysis of GATA-1-regulated miRNAs reveals miR-23a to be a positive modulator of erythropoiesis. Nucleic acids research. 41(7):4129-43.
miRNAs play important roles in many biological processes, including erythropoiesis. Although several miRNAs regulate erythroid
differentiation, how the key erythroid regulator, GATA-1, directly orchestrates differentiation through miRNA pathways remains
unclear. In this study, we identified miR-23a as a key regulator of erythropoiesis, which was upregulated both during erythroid
differentiation and in GATA-1 gain-of-function experiments, as determined by miRNA expression profile analysis. In primary
human CD34+ hematopoietic progenitor cells, miR-23a increased in a GATA-1-dependent manner during erythroid differentiation.
Gain- or loss-of-function analysis of miR-23a in mice or zebrafish demonstrated that it was essential for normal morphology
in terminally differentiated erythroid cells. Furthermore, a protein tyrosine phosphatase, SHP2, was identified as a downstream
target of miR-23a that mediated its regulation of erythropoiesis. Taken together, our data identify a key GATA-1–miRNA axis
in erythroid differentiation.